Sterilization of Biofilm on a Titanium Surface Using a Combination of Nonthermal Plasma and Chlorhexidine Digluconate.

Nosocomial infections caused by opportunistic bacteria pose major healthcare problem worldwide. Out of the many microorganisms responsible for such infections, Pseudomonas aeruginosa is a ubiquitous bacterium that accounts for 10-20% of hospital-acquired infections. These infections have mortality rates ranging from 18 to 60% and the cost of treatment ranges from $20,000 to $80,000 per infection. The formation of biofilms on medical devices and implants is responsible for the majority of those infections. Only limited progress has been made to prevent this issue in a safe and cost-effective manner. To address this, we propose employing jet plasma to break down and inactivate biofilms in vitro. Moreover, to improve the antimicrobial effect on the biofilm, a treatment method using a combination of jet plasma and a biocide known as chlorhexidine (CHX) digluconate was investigated. We found that complete sterilization of P. aeruginosa biofilms can be achieved after combinatorial treatment using plasma and CHX. A decrease in biofilm viability was also observed using confocal laser scanning electron microscopy (CLSM). This treatment method sterilized biofilm-contaminated surfaces in a short treatment time, indicating it to be a potential tool for the removal of biofilms present on medical devices and implants.

Orthopedic complications in diabetes.

Diabetes is associated with a number of lower extremity orthopedic conditions and complications including fractures, Charcot neuroarthropathy, plantar ulcers, and infection. These complications are of significant clinical concern in terms of morbidity, mortality, and socioeconomic costs. A review of each condition is discussed, with particular emphasis on the clinical importance, diagnostic considerations, and orthopedic treatment recommendations. The goal of the article is to provide a clinical picture of the challenges that orthopedic surgeons confront, and highlight the need for specific clinical guidelines in diabetic patients.

Oxford hip scores at 6 months and 5 years are associated with total hip revision within the subsequent 2 years.

BACKGROUND: The Oxford hip score (OHS) is commonly reported in research studies as a reflection of pain and function but it is unclear whether it predicts subsequent prosthesis failure. QUESTIONS/PURPOSES: We determined whether OHS obtained at 6 months and 5 years after surgery predicts risk of revision within the subsequent 2 years. METHODS: We reviewed data from the New Zealand Joint Registry between January 1999 and December 2010. OHS at 6 months was available for 17,831 total hip patients. Patients were separated into four categories based on their OHS: 10,458 (59%) scored 42-48, 4726 (26%) scored 34-41, 1592 (9%) scored 27-33, and 1028 (6%) scored 0-26. Five-year OHSs were available for 3665 patients. Of these patients, 2619 (72%) scored 42-48, 657 (18%) scored 34-41, 225 (6%) scored 27-33, and 164 (4%) scored 0-26. RESULTS: For patients with a 6-month OHS, revision risk within 2 years was 0.4% in the 42-48 group, 1.0% in the 34-41 group, 1.7% in the 27-33 group, and 6.2% in the 0-27 group. For patients with 5-year OHS, revision risk within 2 years was 0.3%, 1.1%, 3.6%, and 6.1%, respectively. Increase in revision risk for the 0-27 versus the 42-48 OHS group was 15-fold at 6 months and 18-fold at 5 years. CONCLUSIONS: Our data suggest patients with an OHS of 42-48 at 6 months need a 5-year postoperative appointment. Those patients with a 5-year OHS of 42-48 need not be followed up for a further 5 years.

Fluoroscopically-guided indirect posterior reduction and fixation of thoracolumbar burst fractures without fusion.

This article presents an evaluation of fluoroscopy for indirect, posterior reduction and fixation of thoracolumbar burst fractures. A prospective study of 25 patients with thoracolumbar burst fractures who underwent C-arm machine-guided posterior indirect reduction and short segment fixation without fusion is described. No laminotomies were performed. All patients had a mean follow-up of 30.4 months. At postoperative review, the average anterior and posterior vertebral heights were corrected from 57.9% to 99.0% and 89.0% to 99.5%, respectively. The Cobb angle was corrected from 18.4 degrees to 0.17 degrees . The canal compromise ratio was improved from 35.2% to 8.6%. In all 25 cases, neurological status was intact at last follow-up. Fluoroscopy guidance is an effective method to accomplish indirect reduction and fixation. Reduction was confirmed on lateral fluoroscopic views by looking for a "one-line sign," which is the reconstitution of the posterior border of the vertebral body.

Use of a 30-degree external rotation view for posteromedial tubercle fractures of the talus.

A fracture of the posteromedial talar tubercle is also referred to as the Cedell fracture and is an infrequently described injury. Failure to recognize this injury may lead to posteromedial ankle pain and tarsal tunnel syndrome. It is therefore important to diagnose these fractures at the time of the initial presentation to avoid future morbidity. Although plain radiography forms the mainstay of initial radiological evaluation of the ankle, these fractures are commonly missed and misdiagnosed because of poor visualization on routine ankle radiographs. Computed tomography helps for better visualization of this fracture at the higher risk of radiation. We evaluated the use of the 30-degree external rotation view for the diagnosis of fractures of the posteromedial tubercle of the talus using cadaver specimens. On the 30-degree external rotation view of the ankle, all fractures of the posteromedial tubercle of the talus were revealed. In contrast, the fracture was visualized in only 2 cases using the standard lateral radiograph of the ankle, and not once in the anteroposterior or mortise views. In conclusion, a 30-degree external rotation view is likely to show a fracture of the posteromedial tubercle of the talus in contrast to the 3 routine trauma views of the ankle, aiding in diagnosis and treatment strategy at time of initial presentation.

Pathomechanism of ligamentum flavum hypertrophy: a multidisciplinary investigation based on clinical, biomechanical, histologic, and biologic assessments.

STUDY DESIGN: A multidisciplinary study involving clinical, histologic, biomechanical, biologic, and immunohistologic approaches. OBJECTIVE.: To clarify the pathomechanism of hypertrophy of the ligamentum flavum. SUMMARY OF BACKGROUND DATA: The most common spinal disorder in elderly patients is lumbar spinal canal stenosis, causing low back and leg pain, and paresis. Canal narrowing, in part, results from hypertrophy of the ligamentum flavum. Although histologic and biologic literature on this topic is available, the pathomechanism of ligamentum flavum hypertrophy is still unknown. METHODS: The thickness of 308 ligamenta flava at L2/3, L3/4, L4/5, and L5/S1 levels of 77 patients was measured using magnetic resonance imaging. The relationships between thickness, age, and level were evaluated. Histologic evaluation was performed on 20 ligamentum flavum samples, which were collected during surgery. Trichrome and Verhoeff-van Gieson elastic stains were performed for each ligamentum flavum to understand the degree of fibrosis and elastic fiber status, respectively. To understand the mechanical stresses in various layers of ligamentum flavum, a 3-dimensional finite element model was used. Von Mises stresses were computed, and values between dural and dorsal layers were compared. There were 10 ligamenta flava collected for biologic assessment. Using real-time reverse transcriptase polymerase chain reaction, transforming growth factor (TGF)-beta messenger ribonucleic acid expression was quantitatively measured. The cellular location of TGF-beta was also confirmed from 18 ligamenta flava using immunohistologic techniques. RESULTS: The ligamentum flavum thickness increased with age, however, the increment at L4/5 and L3/4 levels was larger than at L2/3 and L5/S1 levels. Histology showed that as the ligamentum flavum thickness increased, fibrosis increased and elastic fibers decreased. This tendency was more predominant along the dorsal side. Von Misses stresses revealed that the dorsal fibers of ligamentum flavum were subjected to higher stress than the dural fibers. This was most remarkably observed at L4/5. The largest increase in ratio observed between the dorsal and dural layer was approximately 5-fold in flexion at L4/5 in flexion. Expression of TGF-beta was observed in all ligamenta flava, however, the expression decreased as the ligamentum flavum thickness increased. Immunohistochemistry showed that TGF-beta was released by the endothelial cells, not by fibroblasts. CONCLUSIONS: Fibrosis is the main cause of ligamentum flavum hypertrophy, and fibrosis is caused by the accumulation of mechanical stress with the aging process, especially along the dorsal aspect of the ligamentum flavum. TGF-beta released by the endothelial cells may stimulate fibrosis, especially during the early phase of hypertrophy.